Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9191
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dc.contributor.authorGilbert, Richard Een
dc.contributor.authorCooper, Mark Een
dc.date.accessioned2015-05-15T22:11:19Z
dc.date.available2015-05-15T22:11:19Z
dc.date.issued1999-11-01en
dc.identifier.citationKidney International; 56(5): 1627-37en
dc.identifier.govdoc10571771en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9191en
dc.description.abstractAlthough the glomerulus, particularly the mesangium, has been the focus of intense investigation in diabetes, tubulointerstitial injury is also a major feature of diabetic nephropathy and an important predictor of renal dysfunction. The renal tubule in diabetes is subject to both direct and indirect pathogenetic influences as a consequence of its position in the nephron and its resorptive function. On exposure to glucose, proximal tubular cells elaborate vasoactive hormones, including angiotensin II and injurious cytokines such as transforming growth factor-beta (TGF-beta), as well as extracellular matrix proteins. In turn, angiotensin II may further increase TGF-beta expression in both proximal tubular and interstitial cells, thus amplifying the stimulus to fibrogenesis in the renal tubulointerstitium. In addition to these mostly direct influences, the renal tubule, particularly its proximal segment, is exposed to glomerular effluent. In the diabetic state, this includes large quantities of advanced glycation end products and glucose and, at later stages in the evolution of diabetic nephropathy, protein, all of which are factors that may induce TGF-beta expression and fibrosis. Diabetic nephropathy should therefore be viewed as a disease affecting the entire nephron. Continued exploration into tubulointerstitial disease in addition to glomerular injury in diabetes may help provide further insights into the pathogenesis of diabetic nephropathy and additional targets for therapeutic intervention.en
dc.language.isoenen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherDiabetic Nephropathies.etiologyen
dc.subject.otherGlucose.metabolismen
dc.subject.otherHumansen
dc.subject.otherIschemia.complicationsen
dc.subject.otherKidney Glomerulus.pathologyen
dc.subject.otherKidney Tubules.pathologyen
dc.subject.otherProteins.metabolismen
dc.subject.otherSorbitol.metabolismen
dc.titleThe tubulointerstitium in progressive diabetic kidney disease: more than an aftermath of glomerular injury?en
dc.typeJournal Articleen
dc.identifier.journaltitleKidney Internationalen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine, West Heidelberg, Victoria, 3081, Australiaen
dc.identifier.doi10.1046/j.1523-1755.1999.00721.xen
dc.description.pages1627-37en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/10571771en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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